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http://purl.uniprot.org/citations/17128265http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17128265http://www.w3.org/2000/01/rdf-schema#comment"The mechanisms by which commensal bacteria suppress inflammatory signalling in the gut are still unclear. Here, we present a cellular mechanism whereby the polarity of intestinal epithelial cells (IECs) has a major role in colonic homeostasis. TLR9 activation through apical and basolateral surface domains have distinct transcriptional responses, evident by NF-kappaB activation and cDNA microarray analysis. Whereas basolateral TLR9 signals IkappaBalpha degradation and activation of the NF-kappaB pathway, apical TLR9 stimulation invokes a unique response in which ubiquitinated IkappaB accumulates in the cytoplasm preventing NF-kappaB activation. Furthermore, apical TLR9 stimulation confers intracellular tolerance to subsequent TLR challenges. IECs in TLR9-deficient mice, when compared with wild-type and TLR2-deficient mice, display a lower NF-kappaB activation threshold and these mice are highly susceptible to experimental colitis. Our data provide a case for organ-specific innate immunity in which TLR expression in polarized IECs has uniquely evolved to maintain colonic homeostasis and regulate tolerance and inflammation."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.org/dc/terms/identifier"doi:10.1038/ncb1500"xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Lee H.K."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Lee J."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Shen C."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Raz E."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Liu Y.T."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Eckmann L."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Ben-Neriah Y."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Alkalay I."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Cojocaru G."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Katakura K."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Shenouda S."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Kagnoff M."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Mo J.H."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/author"Rucker A.N."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/name"Nat Cell Biol"xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/pages"1327-1336"xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/title"Maintenance of colonic homeostasis by distinctive apical TLR9 signalling in intestinal epithelial cells."xsd:string
http://purl.uniprot.org/citations/17128265http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/17128265http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17128265
http://purl.uniprot.org/citations/17128265http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17128265
http://purl.uniprot.org/uniprot/Q9NR96#attribution-CCFF90B00F9044A38329958FC7CDCE99http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17128265